Acrivon Therapeutics, Inc. · NASDAQ:ACRV
Acrivon Therapeutics — Investor Presentation (March 2026)
48 slides from Acrivon Therapeutics's investor presentation, Mar 19, 2026
Slide 1: Acrivon Predictive Precision Proteomics (AP3) Corporate Presentation March 2026
ACRIVON PREDICTIVE PRECISION PROTEOMICS (AP3) NEXT GENERATION PRECISION MEDICINE CORPORATE PRESENTATION MARCH 2026 Exhibit 99.2
Slide 2: Forward-looking statements
Forward-looking statements Certain information contained in this presentation includes forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 regarding our future results of operations or financial condition, business strategy and plans and objectives o
Slide 3: Next-generation precision medicine powered by AP3
next-generation precision medicine powered by AP3 Drug P Acrivon Predictive Precision Proteomics (AP3) AI-driven, proteomics-based rational drug design and informed clinical development AP3 enables an exact match between the disease-driving, dysregulated pathways with drug mechanism of action (Acriv
Slide 4: Acrivon therapeutics overview
Development Site (Boston) Drug development and clinical biomarkers Clinical leadership and trial oversight ML/AI-driven AP3 analyses Precision Proteomics Site (Lund/Copenhagen) Early drug discovery BM identification and drug profiling AP3 mass spectrometry Acrivon therapeutics overview Peter Blume-J
Slide 5: Accomplished leadership team
Accomplished leadership team Peter Blume-Jensen, M.D., Ph.D. CEO, President, Co-Founder Eric Devroe, Ph.D. Chief Operating Officer Erick Gamelin, M.D., Ph.D. Chief Development Officer Executive Serono, Merck & Co., Daiichi Sankyo CSO Metamark - Marketed prostate proteomic test ProMark® Inventor Acri
Slide 6: Acrivon Pipeline
Acrivon Pipeline Anticipated Next Milestone Phase 3 Phase 2 Phase 1 Preclinical ACR-368 (CHK1/CHK2) Single-Arm Trial Based on OncoSignature Biomarker Prediction Clinical Data & Dose Expansion Start, 2026 Clinical Update Mid-2026 Endometrial Cancer AP3-Identified Tumor Types Future Development Candid
Slide 7: Acrivon AP3-based precision medicine
Acrivon AP3-based precision medicine AP3 Clinical Biomarkers Predictive OncoSignature tests Single agent activity Target/pathway addiction Resistance Mechanisms Rational drug combinations Drug Discovery SAR Optimized pathway effects PD Markers ~60,000 per compound Informed in-licensing AP3 profiling
Slide 8: The AP3 approach is modality and disease agnostic
Infectious, CNS, and other diseases Oncology Fibrotic and inflammatory Autoimmune DDR and Cell Cycle Therapeutic areas Therapeutic modalities Small molecule Bifunctional molecule Antibody ADC Oligo/RNA The AP3 Approach is modality and disease agnostic Current pipeline Next
Slide 9: ACR-368: a potent selective CHK1/2 inhibitor
ACR-368: a potent selective CHK1/2 inhibitor Balanced potent (nM) inhibition of CHK1 and CHK2 enabling monotherapy activity Protected by composition-of-matter and salt form patents through 2030 and 2037, ensuring exclusivity Acrivon holds full, unencumbered global rights Clinical efficacy and safety
Slide 10: OncoSignature: Drug response prediction in individual patients
Oncosignature: Drug response prediction in individual patients PROPRIETARY WORKFLOW STEP 1 STEP 2 STEP 3 BIOMARKER IDENTIFICATION THERAPEUTIC PACKAGE Acrivon drug with predictive BM assay PATIENT RESPONDERS Optimal indications and combinations AP3 DRUG PROFILING Resistant Sensitive BIOMARKER VALIDAT
Slide 11: AP3 indication finding identifies endometrial cancer as sensitive to ACR-368
ap3 indication finding identifies endometrial cancer as sensitive to ACR-368 ACR-368 OncoSignature-based indication finding prior to trial entry Functional validation in preclinical models BM1 BM2 BM3 ~30% ~70% Clinical validation in ongoing Phase 2 study Endometrial patient tumor samples Predicted
Slide 12: Acrivon CLIA Laboratory
Acrivon CLIA Laboratory Strengthening acrivon precision medicine capabilities Newly licensed CLIA laboratory Translates AP3-driven biomarker discoveries into actionable and proprietary CDx for our therapeutics Initially focused on ACR-368 OncoSignature testing Unique capabilities to support internal
Slide 13: BM-Stratified Cohorts with Prospective Response Prediction
BM-Stratified Cohorts with Prospective Response Prediction Subjects with high-grade EC ≤3 lines of prior therapy The ACR-368 OncoSignature™ is a tumor agnostic, functional Biomarker (BM) test designed to prospectively predict benefit from ACR-368 (prexasertib), a potent, selective CHK1/2 inhibitor.
Slide 14: Significant Response in Arm 1 (BM+)
* Best of BICR and/or PI # Unconfirmed PR Non QC’ed data based on EDC data extract as of 12/04/2025 # # ORR = 39% (95% CI, 24 - 56) n = 31 DCR: 80.6%, CBR (16 weeks): 61.3% BOR by RECIST 1.1 on study treatment* Best overall response (BOR) DCR: Disease Control Rate (CR+PR+SD) CBR: Clinical Benefit R
Slide 15: Arm 1 (BM+) and Arm 2 (BM-) response rates
# # # n = 25 n = 35 ORR = 26% (95% CI, 14 - 42) ORR = 44% (95% CI, 27 - 63) Arm 1 (BM+) ACR-368 ARM 2 (BM-) ACR-368 + ULDG BOR by RECIST 1.1 on study treatment* * Best of BICR and/or PI # Unconfirmed PR Non QC’ed data based on EDC data extract as of 12/04/2025 Better ORR Observed in Subjects with ≤2
Slide 16: Significant ORR in Serous All-Comer Population with ≤2 Prior Lines
# # # n = 23 n = 37 Serous (≤ 2 Prior Lines) Non-Serous (≤ 2 Prior Lines) ORR = 22% (95% CI, 11 - 37) ORR = 52% (95% CI, 33 - 71) DCR: 74%, CBR (16 weeks): 65% BOR by RECIST 1.1 on study treatment* * Best of BICR and/or PI # Unconfirmed PR Non QC’ed data based on EDC data extract as of 12/04/2025 S
Slide 17: Deep, rapid responses in aggressive serous endometrial tumors
Screening Week 8 Week 12 Complete resolution of hepatic target lesions (-100%) (-100%) Deep, rapid responses in patients with aggressive serous endometrial tumors Screening Week 8 and 12 (-100%) Confirmed PR with complete disappearance of >10 additional hepatic metastases spanning both lobes ACR-368
Slide 18: Serous endometrial cancer - a significant unmet need
Serous endometrial cancer - a significant unmet need Disproportionate Mortality Accounts for ~40-50% of all endometrial cancer deaths.5 Limited Effective Treatment Options Only moderate benefit from immunotherapy Chemotherapy responses short-lived. Rapid resistance, early recurrence. HER2-targeting
Slide 19: Treatment-Related Adverse Events
Treatment-Related Adverse Events N = number of subjects (%) Arm 1 (ACR-368) N=40 Grades 3/4 Arm 2 (ACR-368 + ULDG) N=48 Grades 3/4 Thrombocytopenia 9 (22) 17 (34) Anemia 11 (27) 22 (46) Leukopenia 6 (15) 11 (23) Neutropenia 10 (25) 16 (33) Febrile neutropenia 2 (5) 4 (8) Acute kidney injury 2 (5) 0
Slide 20: Endometrial patient demographics and baseline characteristics
Endometrial patient Demographics and baseline characteristics Subject Demographics BM+ N = 40 BM- N = 48 Median Age (range) 66.0 (40, 77) 66.0 (49, 80) Race, n (%) White 29 (72.5) 29 (60.4) Black/African American 6 (15) 10 (20.8) Asian 1 (2.5) 4 (8.3) American Indian or Alaska Native 0 0 Native Hawa
Slide 21: ACR-368 registrational intent program design
Subjects relapsed after prior platinum-based chemotherapy and one prior line of anti-PD-(L)1 therapy Arm 1 BM+ N=71 ACR-368 Arm 2 BM- N= up to ~150 ACR-368 with ULDG sensitization Biopsy-Independent Serous Cohorts (US + EU) Subjects with ≤2 lines of prior therapy Arm 3 Serous All-Comer N= up to ~90
Slide 22: Potent synergy of ACR-368 with anti-PD-L1 displays immune memory
Potent synergy of ACR-368 with anti-PD-L1 displays immune Memory in 100% of Mice Complete tumor regression Immune memory Immune memory independent of CD8 Immune memory independent of CD4 Immune memory Co-mediated by CD4 + CD8 Legends:
Slide 23: Development path for ACR-368 in endometrial cancer
Development path for ACR-368 in endometrial cancer Registrational intent Phase 2 single arm study of ACR-368 monotherapy in all BM+ EC patients All endometrial subtypes Enrollment completion (N =71 BM+ subjects) anticipated 2027 Registrational intent Phase 2 single arm study of ACR-368 with ULDG as
Slide 24: ACR-368 + Anti PD-1 confirmatory phase 3 trial
ACR-368 + Anti PD-1 confirmatory phase 3 trial Placebo Carboplatin AUC 5 mg/mL/min Paclitaxel 175 mg/m2 Q3W for 6 cycles ACR-368 Q2W plus Anti PD-1 Q6W Placebo plus Anti PD-1 Q6W Follow- up R1:1 Eligible patients Subjects with advanced stage (III, IVA, or IVB) or recurrent pMMR EC with measurable di
Slide 25: ACR-368 offers multiple attractive opportunities
Monotherapy ULDG Sensitization PD1 Combination PD1/VEGF Bispecific Combination ADC Combination Endometrial MDS/MPN, HPV+ SCC, H&N, GBM Future Indications Initial Focus Broad Indication and Combination Expansion Opportunities acr-368 offers multiple attractive opportunities ACR-368-201 Arm 1 Biomarke
Slide 26: Internal pipeline: AP3-based drug discovery
Internal pipeline: AP3-based drug discovery potential first- and best in class candidates Streamlined AP3-based drug discovery AP3 used for biologically relevant selectivity profiling ACR-6840: Development candidate, novel CDK11 inhibitor Anticipated IND filing Q4 2026 Multiple equally promising bac
Slide 27: WEE1 and PKMYT1 - critical cell cycle checkpoints
Wee1 and PKMYT1 - critical cell cycle checkpoints in human cancer WEE1 and PKMYT1 regulate S and G2-M cell cycle checkpoints to ensure proper DNA replication and mitotic completion Defective DNA repair is highly prevalent in cancers, creating a dependency on checkpoint proteins Demonstrated clinical
Slide 28: ACR-2316 is a potentially best- and first-in-class agent
Acr-2316 is a potentially best- and first-in-class agent designed using Acrivon’s ap3 platform Program Goals Demonstrated Results Superior single agent activity High selectivity and potency Streamlined clinical development Favorable ADME-PK, Therapeutic Index, and tolerability profile Broad preclini
Slide 29: ACR-2316 is highly potent across tumor cell lines and ex vivo models
ACR-2316 is highly potent across human tumor cell lines and patient-derived ex vivo tumor models Patient-derived ex vivo ovarian tumor models Human tumor cell lines (not genetically selected) Breast Lung Ovarian Prostate Renal Medulloblastoma Glioblastoma Pancreatic WEE1i PKMYT1i
Slide 30: Superior activity of ACR-2316 over WRN inhibitors
SUPERIOR ACTIVITY OF ACR-2316 oVER WRN INHIBITORS IN BOTH MSI HIGH AND MSS CELL LINES HRO761 is a noncovalent allosteric inhibitor of WRN (Novartis); VVD-133214/ RO7589831 is a covalent allosteric WRN inhibitor (Roche); ACR-2316 is more potent than both WRN inhibitors even in the optimal MSI high co
Slide 31: ACR-2316 induces complete tumor regression across models
ACR-2316 induces complete tumor regression across models and dosing regimens 5d on/2 d off Model 1 5d on/2 d off Model 2
Slide 32: Phase 1 dose escalation and expansion design
Phase 1 Dose Escalation and Expansion Design Cohort A 3on/4off Cohort B 2on/5off Dose Level 1 Dose Level 2 Select tumor types Dose Escalation 30 mg 200 mg 240 mg 120 mg 60 mg 240 mg Cohort C 2on/12off 360 mg TBD 280 mg 160 mg Dose Expansion ✅ ✅ Two weekly oral regimens (3d on/4d off and 2d on/5d off
Slide 33: ACR-2316 shows promising clinical activity in lung cancer
ACR-2316 shows promising clinical activity in lung cancer during dose escalation Non-QC’ed EDC data extract 3/3/2026 Two weekly oral dosing schedules established; Clinical activity observed at ≥120 mg DCR (Target lesion) across all tumor types 79% Initial clinical activity and DCR (6/7) observed in
Slide 34: Favorable tolerability profile
Favorable tolerability profile summary of ≥ grade 3 TRAEs # Subjects; % Total Gr. 3 N=20 Total Gr. 4 N=20 Total Gr 3/4 N=20 Neutropenia/neutrophil count decreased 4; 20% 1; 5% 5 25% Leukopenia/white blood cell count decreased 1; 5% 1; 5% 2; 10% Anaemia 1; 5% 0 1; 5% Lymphocyte count decreased 0 0 0
Slide 35: Demographics and baseline characteristics
Demographics AND BASELINE CHARACTERISTICS Non QC’ed data based on EDC data extract as of 12/22/2025 Subject Demographics N = 33 ECOG Status at Baseline, n (%) 0 10 (30) 1 23(70) Prior Lines of Therapy, n (%) 1 1 (3) 2 5 (15) 3 14 (42) 4 7 (21) 5 2 (6) 6 2 (6) 7 1(3) 8 1(3) Prior exposure to IO thera
Slide 36: Potent synergy of ACR-2316 with anti-PD-L1 displays immune memory
Potent synergy of ACR-2316 with anti-PD-L1 displays immune Memory in 100% of Mice Legends: Complete tumor regression Immune memory Immune memory independent of CD8 Immune memory independent of CD4 Immune memory co-mediated by CD4 + CD8
Slide 37: Potential development paths for ACR-2316
Potential development paths for ACR-2316 AP3-predicted solid tumor types of high unmet need, e.g. SCLC, sqNSCLC, HPV+ tumors, etc. Single agent 2nd/3rd line Chemo combination (DDR stress sensitization in earlier lines) Weekly and bi-weekly dosing regimens provide flexibility for combinations, includ
Slide 38: New preclinical development candidate ACR-6840: CDK11 inhibitor
New preclinical cell cycle development candidate ACR-6840: potential first-in-class CDK11 inhibitor No clinical-stage competitors Attractive cancer cell cycle drug target, well-suited for AP3 platform, multiple protein isoforms Broad role in cell cycle control and oncogenesis; CDK11 controls transcr
Slide 39: AP3 generative phosphoproteomics platform
AP3 Generative phosphoproteomics platform Structured Standardized AI-enabled AP3 Interactome AP3 KSR Predictor AP3 Data Portal AP3 Chatbot Proprietary Database Drug design and optimization Target ID / Indication Finding MoA / response prediction PD and predictive biomarkers MS-proteomics Functional
Slide 40: AP3 interactome: proprietary data analysis infrastructure
Data completeness Peptide IDs CV Pearson Correlation PCA Hierarchical Clustering DEPs Volcano Plots ANOVA Hierarchical clustering Consensus Sequence Motif Kinase Inference Pathway Enrichment Network Mapping Biomarkers Machine-Learning Filtering Batch effects Normalization Imputation ~164,000 phospho
Slide 41: AP3 reveals drug-regulated kinase activity in intact cells
AP3 reveals drug-regulated kinase activity in intact cells not detectable by standard methods Time : 60 minutes Dose : 20 nM KinomeScan @ 1mM ACR-2316 Drug-regulated kinase activity* in intact cells ACR-2743 (previous lead candidate) *Kinase activity based on substrate motif analysis using a proprie
Slide 42: AP3 reciprocal quenching identifies PKMYT1 as WEE1 inhibitor resistance mechanism
AP3 Reciprocal quenching identifies PKMYT1 as a key wee1 inhibitor-induced resistance mechanism Induced Suppressed Enrichment Score (NES) 500 5 Protein set size Mitotic regulation Cell cycle and cancer DNA homology repair DNA damage responses Sensitive Resistant WEE1i PKMYT1i PKMYT1i WEE1i PUJANA_BR
Slide 43: Reciprocal quenching reveals optimal potency profile for dual WEE1/PKMYT1 inhibitor
AP3 reciprocal quenching reveals optimal target potency profile for dual WEE1/PKMYT1 inhibitor PKMYT1i WEE1i PKMYT1i WEE1i Sensitive Resistant HCL, Euclidean 1043 p-sites from 298 proteins 4 -4 Centered log2FC (treated vs. DMSO) Target substrate of ACR-368 Target substrate of PKMYT1i Optimal potency
Slide 44: ACR-2316 induces activation of pro-apoptotic mitotic kinases
Acr-2316 induces potent activation of pro-apoptotic mitotic kinases in sensitive tumor cells Robust activation of CDK1with ACR-2316 exemplified by enrichment of 206 upregulated substrates of CDK1 ACR-2316 @60min and 200nM in ACHN
Slide 45: Potent inhibition of CDK1 consensus substrate Y15 by ACR-2316
Robust potent inhibition of CDK1 consensus substrate Y15 by ACR-2316 AP3 interactome enables real time quantitative computational analyses of proprietary AP3 drug profiling data across different conditions and experiments Comparison @60min and 200nM in ACHN Time-dependent comparison @ 200nM in ACHN
Slide 46: AACR 2025: Generative Phosphoproteomics
AACR 2025: Generative Phosphoproteomics AP3 uncovers robust tumor cell death through cdk1, cdk2, and plk1 Poster link here
Slide 47: Data driven execution and value creation
data driven execution and value creation Recent Accomplishments (Last 12 Months) Anticipated Next Milestones (2026) Continued positive ACR-368 data in ongoing registrational intent EC trial (April 2025 and January 2026 Corporate R&D Events) Two weekly oral dosing regimens for ACR-2316; promising cli
Slide 48: Financial highlights
FINANCIAL HIGHLIGHTS Approximate Cash and Investments $118.6M Projected runway into Q2 2027 Approximate Fully Diluted Shares Outstanding 45.1M Current operating plan, assuming no additional financing Balance sheet 31-Dec-2025 Shares, pre-funded warrants, and equity grants outstanding 31-Dec-2025 Not
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